Oral Glucose Tolerance Test Report

Oral Glucose Tolerance Test ReportJason TaylorIntroductionGlucose is a simple sugar that provides nearly half of the bodys energy, it ratt be eaten directly thus it is obtained from eating foods that contain carbohydrates. The colored barge ins about 1/3 of the bodys total glucose in the form of glycogen patch muscle cells store 2/3 of glucose in the same form (Whitney Rolfe, p99). The amount of sugar present in the declension is k nary(prenominal)n as the bank line sugar, these levels need to be tightly regulated by the body (Jiang Zhang 2003). Eating food causes an emergence in race glucose levels, this stimulates insulin release from the pancreas into the blood stream, insulin stimulates glucose uptake into cells, stimulates colored and muscle cells to store it as glycogen and then the excess glucose is converted into fat (Whitney Rolfe, p99). subaltern blood glucose levels be stimulated by the glucagon release from the pancreas, this causes the stored glycogen to b e converted to glucose which causes an gain in the blood glucose levels (Whitney Rolfe, p99).Diabetes Mellitus is a group of disorders that know glucose in perimeter in common, type I and type II diabetes are the most common. type I diabetes mellitus is when the cells dont produce decent insulin and its symptoms include excessive thirst and urination, lethargy, unexplained weight loss and wounds that bring round slowly. Type I diabetes is due to the loss of beta cells in the pancreas which are responsible for the secretion of insulin (McCance Huether, pg745). There pass water been two types of type I diabetes identified, type 1A is an autoimmune disease in which environmental and transmissible factors innovation the destruction of beta cells. Type 1B is non-immune and its when individuals having varying amounts of insulin deficiency (McCance Huether, pg746). Type II diabetes mellitus is less common and is when cells dont respond to insulin, genetic factors such as a lack of insulin receptors combined with environmental influences care obesity can forget in the pathophysiologic mechanisms for type II diabetes like decreased insulin secretion and insulin resistance. These are crucial for the development of type II diabetes mellitus (McCance Huether, pg750).There are numerous complications associated with diabetes such as hypoglycaemia, hyperglycaemia and diabetic ketoacidosis. Hypoglycaemia is when thithers low levels of glucose which is damaging as the idea and nervous system rely on glucose to function. Hypoglycaemia can be caused by too much insulin, strenuous physical exertion or inadequate food intake (Munter Spiegelman, 2007). Impaired glucose regulation can decease to hyperglycaemia which is abnormally high levels of glucose in the blood, for this to occur at to the lowest degree 80-90% of the beta cell function have to be compromised (McCance Huether, pg758).Carbohydrates need to be broken down into monosaccharaides before they can b e absorbed. Their digestion begins in the lecture when salivary amylase hydrolyses them to shorter polysaccharides, they then progress to the stomach that doesnt play a role in carbohydrate digestion as as yet its low pH inactivates the salivary amylase (Whitney Rolfe, p101). The small intestine is where most of the digestion occurs, pancreatic amylase breaks down the polysaccharides to monosaccharides which are then absorbed (Whitney Rolfe, p103).A glucometer is used to calculate the immersion of glucose in the blood, a small drop of blood or a sample is placed on a disposable strip which is inserted into the glucometer which calculates the blood sugar levels (Whitney Rolfe, 2013). An oral glucose tolerance test (OGTT) is used to detect diabetes mellitus, in that location are accepted minimum and maximum values for glucose levels in blood (mmol/L) to be within, if they are beneath or exceed them it could indicate a diabetic profile.In this report we investigated the presenc e of glucose in peeing samples as well as the BGL in prepared samples to determine if any of the patients showed a diabetic profile.MethodsMost of the methods were followed as stated in RMB2530 Pathophysiology 1 testing ground Manual, 2013 however due to safety and health issues real blood and urine samples were not taken.Results tally-in 3 Class Glucose Tolerance Test Results (Mary)Table 3 Class Glucose Tolerance Test Results (Alex)Graph 1 air Glucose Vs. Time for Mary and AlexDiscussionMary had a normal OGTT result as her blood glucose levels didnt have a dramatic increase and they decreased efficiently as well. Marys blood glucose rose at 30 minutes (6.06 mmol/L) however the liver responded to the extra glucose by releasing insulin which promoted the uptake of glucose by cells and its storage as glycogen (Rubin Strayer, pg680). Alex had an stricken reception to glucose as his glucose levels rose at 30 minutes and unbroken rising till 60 minutes, his highest glucose readi ng was 16 mmol/L piece of music Marys highest was 6 mmol/L. From 60 minutes onwards Alexs blood glucose exceeded the maximum send acceptable for blood glucose levels. At 60 minutes his blood glucose was 17.16 mmol/L while the maximum accepted range is 8.9 mmol/L. This indicates a diabetic profile as a normal response is insulin release by the pancreatic beta cells that regulate glucose uptake in liver and skeletal muscle. The delayed decline in glucose suggests that the beta cells arent producing glucose or that the cells arent responding to the insulin (Rubin Strayer, pg1090).The liver is the primary organ involved in glucose homeostasis responding rapidly to fluctuation in blood glucose levels. The reason that there is an increase in blood glucose is due to the consumption of food. Eating foods causes an increase in blood glucose, this stimulates the release of insulin by the pancreas which is responsible for stimulating glucose uptake. Excess blood glucose is utilised by the b ody and stored as glycogen in liver and skeletal muscle while excess glucose is converted to fat (Whitney Rolfe, p99). During periods of starving or fast, there is a lack of glucose. Low blood glucose levels are stimulated by the glucagon release from the pancreas, this causes the stored glycogen in the liver to be converted to glucose which causes an increase in the blood glucose levels. The conversion of glucose to glucose is known as glycogenolysis, gluconeogenesis is formation of glucose from non-carbohydrate sources such as amino acids and fatty acids and is utilised during fasting periods. Symptoms of patients with diabetes mellitus include excessive urination and thirst, lethargy, headaches, dizziness, mood swings and leg cramps.Type I and II are the most commonly known diabetes forms however there are other types. Some people dont have high enough blood glucose levels to be classified as diabetes, however since they are not normal its known as impaired glucose metabolism or pre-diabetes. There are two pre-diabetic conditions impaired glucose tolerance (IGT) and impaired fasting glucose (IFG). IGT is when glucose levels are not high enough to be classified as diabetes, however they are still high while IFG are when blood fasting glucose levels escalated during fasting states but are yet again not high enough to be classified as diabetes. Gestational diabetes is a high blood glucose level during pregnancy as a result of the hormones, it usually goes away after the babys birth. Excessive thirst with large amounts of diluted urine is known as diabetes insipidus (DI), it occurs in two forms central diabetes insipidus (CDI) and nephrogenic diabetes insipidus (NDI). CDI is due to an ADH deficiency, ADH or anti-diuretic hormone is responsible for retaining water. NDI is when the kidneys or nephrons are insensitive to ADH.Glycosuria is the presence of glucose in the urine, glucose is usually filtered back into the bloodstream by the kidneys. Untreated diabet es mellitus is due to high-flown glucose levels which leads to glycosuria. Filtrate pass by sieves in the kidney walls and get reabsorbed in to the blood. revile to the filters results in filtrate excretion into urine. Urine sample A belonged to Alex and was compulsive for glucose as it changed from blue (negative) to dark green (+). Urine sample B belonged to Mary and it was negative for glycosuria. Alexs positive urine sample could be due to his elevated glucose levels.Any differences between individual results could be attributed to a number of different reasons, there could have been errors during the glucometer readings such as dirty the glucometer stick. There could have been errors made during the pipetting of the stock glucose and water resulting in a different concentration to what was required. The experiment should be repeated again to add rigor to the results.Overall the experiment followed scientific expectations, the patient with diabetes mellitus was identified through measurement of the blood glucose levels as well as testing of a urine sample. The experiment should be repeated again to add validity to the results.ReferencesTortora, GJ, Funke, BR, Case, CL (2010).Microbiology An Introduction. 10th ed. San Francisco Pearson Benjamin Cummings. 318, 586, 587, 710.McCance, KL, Huether, SE, Brashers, VL, Rote, NS (2010).PathophysiologyThe biological Basis for Disease in Adults and Children. 6th ed. Missouri Mosby Inc . 296, 1684.Rubin, R, Strayer, DS (2012).Rubins Pathology Clincopathologic Foundations of Medicine. 6th ed. Baltimore Lippincott Williams Wilkins. 332, 346, 348.Jiang, G. Zhang, B.B. 2003, Glucagon and regulation of glucose metabolism,American journal of physiology. Endocrinology and metabolism,vol. 284, no. 4, pp. E671-678.Whitney, E Rolfes, S (2012).Understanding Nutrition. 13th ed. Australia New Zealand Yolanda Cassio. Pg95-101.